An exciting new finding suggests that a specific enzyme in the brain is responsible for blocking the creation of new memories in Alzheimer's patients. And stopping that enzyme has already reversed Alzheimer's symptoms in mice. This could be a major breakthrough.

A team of neuroscientists at MIT say they have identified a particular enzyme known as HDAC2 that is massively overproduced in the brains of those suffering from Alzheimer's disease. This particular enzyme is part of a family collectively known as the Histone deacetylases, or HDACs. These enzymes control gene regulation through the histones, which are proteins closely involved in reinforcing the chromatin structure of DNA strands. Basically, the HDACs can alter the expresion of histones so that certain regions of the chromatin become tighter, cutting off the expression of genes in the affected area.

The researchers found that one particular HDAC enzyme, HDAC2, was all over the hippocampus region of the brain in Alzheimer's affected mice. That makes sense, considering previous research has linked HDAC2 to the regulation of memory and learning. In this case, it seems that the presence of far too much HDAC2 was forming a sort of "gene blockade" that prevented any of the genes responsible for memory creation from working properly.

When the neuroscientists inhibited this enzyme, the Alzheimer's symptoms disappeared in the mice, and their brains started creating memories again. Research leader Li-Huei Tsai explains what is going on inside the mice's brains:

"It's not just one or two genes, it's a group of genes that work in concert to control different phases of memory formation. With such a blockade, the brain really loses the ability to quickly respond to stimulation. You can imagine that this creates a huge problem in terms of learning and memory functions, and perhaps other cognitive functions. This result really advocates for the notion that if there is any agent that can selectively down-regulate HDAC2, it's going to be very beneficial."

The researchers estimate that it will take at least ten years to develop an effective treatment for human Alzheimer's patients using this new breakthrough, but the early indications are that this should be a promising line of research. For one thing, autopsies of deceased Alzheimer's patients indicate excess amounts of HDAC2 in both the hippocampus and the entorhinal cortex, both of which are vital to memory creation. That suggests that the same basic phenomenon observed in the research mice is also going on in human brains — which is great news for a potential treatment.